The goal of the Human Genome Project was to map and sequence the entire human genome. It was with great anticipation that the scientific community awaited the completion of the human genome project, as this information will revolutionize modern medicine in ways that we are only starting to realize. Of immediate consequence is the enormous impact that the completed sequence will have on the lengthy and extremely laborious process of mapping and cloning disease loci. There is no doubt that the availability of the sequence will shorten and simplify this process, and that in the next 10 years many of the genes underlying the approx 12,000 genetic diseases known will be mapped and perhaps cloned.

The identification of the genes responsible for inherited disorders is a key first step toward understanding the biological processes affected. With these genes at hand it is then possible to generate animal models, which are powerful tools to unravel the etiology of each disorder and therefore to devise treatments. Even though there are numerous encouraging prospects, and a few successes, many of the studies of animal models of brain genetic disorders are in their infancy, and they have yet to yield useful therapies. Here, we review how molecular, physiological, and behavioral studies in animals are starting to elucidate the molecular and cellular basis for cognition. We also discuss how these multilevel integrative studies in animal models can shed light on the etiology of the cognitive deficits associated with genetic disorders in humans. We focus on the role of mouse genetics and use as an example the work that has been done with mouse models of neurofibroma-tosis type 1 (NF1), one of the most common single-gene disorders to cause

From: Contemporary Clinical Neuroscience: Genetics and Genomics of Neurobehavioral Disorders Edited by: G. S. Fisch © Humana Press Inc., Totowa, NJ

learning deficits. We also discuss how these studies can lead to insights into possible therapies.

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